CR PBLs Flashcards

1
Q

Types of CoA

A

Pre-ductal
Juxtaductal
Post-ductal

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2
Q

Which type of CoA is most common?

A

Juxtaductal

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3
Q

Defects associated with CoA

A

Left sided obstructive defects
VSD
Bicuspid aortic valve
Aortic arch hyperplasia

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4
Q

Surgical treatments for CoA

A

Resection and end-end anastomosis
Patch aortoplasty
Left subclavian flap angioplasty
Bypass graft repair

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5
Q

Symptoms of second degree heart block

A

Lightheadedness, dizziness, syncope
Chest pain
Irregular heart beat
Bradycardia

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6
Q

Causes of heart block

A
Electrolyte imbalances 
MI 
Coronary artery disease
Myocarditis or cardiomyopathy 
Heart enlargement from heart failure
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7
Q

Indications for pacemaker in heart block

A

Persistant bradycarida
Asystole for >3 seconds
Heart failure
Associated with neuromuscular disease

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8
Q

When is CRP commonly raised?

A

Late pregnancy
Mild inflammation
Bacterial and viral infection
Burns

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9
Q

Reversible risk factors or angina

A
Smoking 
Hypertension 
Hyperlipidameia 
Obesity 
Physical inactivity
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10
Q

Irreversible risk factors for angina

A

Family history
Older age
Male sex
Diabetes mellitus

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11
Q

Signs of angina on ECG stress test

A

ST depression
T wave inversion
Short and spikey T waves

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12
Q

Drugs used in angina treatment

A
Aspirin
CCBs
BBs
Statins 
Nitrates 
Beta blockers 
ACEIs
ARBs
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13
Q

Characteristics of unstable angina

A

Pain comes on suddenly
Not triggered by exertion
Does not go away with rest
Gets worse over a short period of time

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14
Q

ST elevation

A

= ongoing active damage
>2mm in chest leads
>1mm in limb leads
Must be present in 2 or more contiguous leads

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15
Q

Pathological Q waves

A
= irreversible damage 
>0.04s
>2 small squares in depth 
>25% of the depth of the QRS complex 
Present in V1-3
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16
Q

Troponin subtypes

A

T and I

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17
Q

When is troponin released and when do levels return to normal?

A

First released 4-6 hours after attack

May remain elevated for 2 weeks

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18
Q

Myocardial creatine kinase

A

= CK-MB

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19
Q

When is CK released and when do levels return to normal?

A

3-12 hours after infarct

Return to normal after 48-72 hours

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20
Q

When is AST released and when do levels return to normal?

A

Peaks around 48 hours

Returns to normal after 5 days

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21
Q

When is LDH released and when do levels return to normal?

A

Peaks around 72 hours

Returns to normal after 6 days

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22
Q

When is myoglobin released?

A

As early as 2 hours after infarct

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23
Q

Pain felt in AMI

A
Intense and consistent for 30-60 minutes
Retrosternal
Radiates --> neck, jaw, back, arm
May be felt as indigestion 
Felt as a weight on the chest as squeezing pain
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24
Q

AMI immediate treatment

A

Aspirin
Pain relief and sedation
Thrombolysis or PCI
Beta blockers

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25
Secondary prevention
Aspirin Beta blocker Statin ACEI
26
Short term complications of AMI
Arrhythmia Heart failure Rupture Mural thrombosis
27
Long term complications of AMI
Aneurysm Heart failure Pericarditis
28
Adverse prognostic features of AMI
``` Advanced age Anterior AMI Larger AMI Heart failure Systolic hypotension Complex ventricular arrhythmias >24h after infarct History of previous infarct(s) ```
29
Causes of heart failure
``` Coronary artery disease Valve disease Cardiomyopathy Congenital defects Toxins (alcohol, cocaine) Drugs (BBs, CCBs) Anaemia Pregnancy Hyperthyroidism ```
30
Major criteria for heart failure
``` PND Weight loss with treatment Neck vein distention Hepatojugular reflux Rales S3 gallop Cardiomegaly ```
31
Minor criteria for heart failure
``` Nocturnal cough Dyspnoea on normal exertion Decrease in VC by 1/3 Pleural effusion Tachycardia Bilateral ankle oedema ```
32
Why do you get PND?
Return of peripheral oedema fluid to circulation due to gravity Reduced respiratory drive during sleep Reduced sympathetic bronchodilation during sleep
33
ECG features of heart failure
LVH (high R waves in V4-6) ST depression showing ischaemia LBBB
34
CXR findings
``` Cardiomegaly Bat wing sign Kerley B lines Pleural effusions Upper lobe diversion ```
35
Echo findings
``` Reduced eject fraction Dilated ventricles Valve dysfunction Pulmonary artery pressure raised Reduced/increased wall thickness ```
36
Drugs for heart failure
``` Diuretics ACEIs Beta blockers ARB Aldosterone blocker Digoxin ```
37
Heart failure prognosis
50% die within 5 years
38
Asthma characteristics
Airflow limitation Airway hyper responsiveness Inflammation on bronchi
39
Raised cells in asthma
Eosinophils Mast cells T cells
40
Signs of severe asthma
``` SaO2 <92% PEFR <33% predicted Tachycardia PaO2 <8kPa PaCO2 normal or raised Silent chest Cyanosis Inability to complete sentences in one breath Feeble respiratory effort ```
41
Treatment ladder of asthma
``` Salbutamol Inhaled steroid LABA Leukotriene antagonist Antimuscarinic Theophylline Oral steroid ```
42
Risk factors for DVT
``` Previous DVT Hospitalisation Surgery Active cancer Lower limb trauma Increasing age Pregnancy COCP/HRT Obesity Thrombophilia Long haul travel Family history ```
43
Signs and symptoms of DVT
``` Limb pain Tenderness Swelling Pitting oedema Distention of superficial veins Increased temperature Erythema Cord like palpable vein ```
44
What is D dimer?
Breakdown product of cross-liked fibrin produced by plasmin
45
DVT treatment
LMWH then warfarin
46
Complications of DVT
PE Active bleeding from treatment Post-thrombotic syndrome Heparin induced thrombocytopaenia
47
Forms of embolus
``` DVT Fat Air Amniotic fluid Tumour ```
48
Symptoms of PE
Dyspnoea Pleuritic chest pain Haemoptysis
49
Atypical symptoms of PE
``` Syncope Seizures Abdominal pain Fever Confusion Delirium ```
50
Signs of PE
``` Tachycardia Tachypnea Hypoxia Pyrexia Raised JVP Pleural rub Accentuated second heart sound Hypotension and shock ```
51
Differential diagnosis of PE
``` Pneumonia Acute coronary syndrome Aortic dissection Cardiac tamponade Pneumothorax ```
52
ECG signs of PE
``` Tachycardia RBBB RV strain RAD Large P waves S1Q3T3 pattern Atrial arrhythmia ```
53
CXR signs of PE
``` Dark lung fields Focal oligaemia Prominent central artery Basal wedge shaped opacities Pleural effusion ```
54
Type of respiratory failure in PE
1
55
Treatment of PE
Heparin or fondaparinux Then warfarin Thrombolysis in massive PE
56
Can thrombolysis be used in pregnancy?
YES
57
Sites of RBC production
Yolk sac Liver and spleen Bone marrow
58
Forms of haemoglobin
Hb Gower 1 = zeta 2 epsilon 2 HbF = alpha 2 gamma 2 HbA = alpha 2 beta 2 HbA2 = alpha 2 delta 2
59
Genetics of alpha thalassaemia
Gene deletions on chromosome 16 | Usually 4 genes present
60
Consequences of alpha thalassaemia
1-2 deletions = no symptoms 3 deletions = HbH disease --> severe microcytic anaemia 4 deletions = hydrops foetalis --> death
61
Hb levels in beta thalassaemia major
Low HbA High HbF Normal or slightly high HbA2
62
Sites of extra medullary haematopoiesis
Spleen | Liver
63
Consequences of haemolysis
Jaundice Reticulocytosis Hepatosplenomegaly
64
Treatment of beta thalassaemia major
Regular blood transfusions Iron chelation therapy Bone marrow transplant Splenectomy
65
Iron chelating agents
Desferrioxamine (SQ) | Deferiprone (oral)